The inhibition of puberty by undernourishment or excessive exercise is of considerable clinical interest. Underlying this phenomenon is a difficult physiological question: "how is puberty regulated metabolically and endocrinologically by body growth, even in the well-nourished female who does not exercise extensively?" Most female mammals experience puberty only when they have achieved a particular body size or composition. This implies a metabolic linkage of some kind between nutrient or energy processing and gonadotropin secretion. We know virtually nothing about this linkage. The object of this proposal is to explore the relationship between food intake, exercise, metabolism, growth, endocrines and puberty in female rats. I have developed a feeding paradigm that allows a great degree of control over the pulsatile secretion of LH. I intend to use this paradigm to determine which dimension of food (calories vs. protein vs. specific amino acids, etc.) actually controls the GnRH pulse generator. Furthermore, I plan to find out whether or not there is a separate and specific, bloodborne, metabolic signal involved in the control of GnRH secretion. My endocrine concerns here are broad: they include both in vivo and in vitro approaches, and the roles played by GH, TSH, FSH, and Prl, as well as LH. As a comparative approach, I intend to study in the same detail the physiological pathways involved in the inhibition of puberty by excessive exercise. I have developed a caging system in which young rats must use a running wheel to obtain their food. Pilot studies suggest that I can inhibit puberty with this system by increasing energy expenditure, even while allowing otherwise normal energy and nutrient intake. Ultimately I want to develop two large sets of data using the feeding and exercise paradigms. Together these two data sets should yield new testable hypotheses about the way puberty is regulated by calories and nutrients in normally growing females.